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Article

SETD2 is required for DNA double-strand break repair and activation of the p53-mediated checkpoint.

eLife - 6 May 2014

Carvalho Sílvia, Vítor Alexandra C, Sridhara Sreerama C, Martins Filipa B, Raposo Ana C, Desterro Joana M P, Ferreira João, de Almeida Sérgio F

Abstract excerpt

Histone modifications establish the chromatin states that coordinate the DNA damage response. In this study, we show that SETD2, the enzyme that trimethylates histone H3 lysine 36 (H3K36me3), is required for ATM activation upon DNA double-strand breaks (DSBs). Moreover, we find that SETD2 is necessary for homologous recombination repair of DSBs by promoting the formation of RAD51 presynaptic filaments. In...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to DNA Breaks, Double-Stranded

Share to Histone-Lysine N-Methyltransferase

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Share to Replication Protein A

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Source

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Identifiers

PMID: 24843002
DOI: 10.7554/eLife.02482
PMCID: PMC4038841

Genes

SETD2
ATM
RAD51

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

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SETD2 is required for DNA double-strand break repair and activation of the p53-mediated checkpoint.PMID 24843002Read ↗

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SETD2 maintains nuclear lamina stability to safeguard the genomeSemantic proximity Read ↗

A New Chromatin-Cytoskeleton Link in Cancer.Semantic proximity Read ↗

Structure/Function Analysis of Recurrent Mutations in SETD2 Protein Reveals a Critical and Conserved Role for a SET Domain Residue in Maintaining Protein Stability and Histone H3 Lys-36 Trimethylation.Semantic proximity Read ↗

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Interplay between H3K36me3, methyltransferase SETD2, and mismatch recognition protein MutSα facilitates processing of oxidative DNA damage in human cellsSemantic proximity Read ↗

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